Lung injury which leads to the adult respiratory distress syndrome (ARDS) is difficult to diagnose early in its course. This is partially because ARDS is masked by mechanical ventilators and partially because of the lung's interdependence with cardiac hemodynamics. Once established, the mortality of ARDS in our Surgical Intensive Care Unit is over 60%. An early morphologic finding in patients dying from ARDS is pulmonary endothelial cell damage. Since the pulmonary vasculr endothelium is known to extract or metabolize specific vasoactive hormones, we propose to study possible alterations in the ability of the pulmonary microvasculature to remove 5-hydroxytryptamine, prostaglandin E1 and prostaglandin F2alpha in control surgical patients and in those who may be prone to develop ARADS. Cardiac surgical patients will be the subjects and will be studied serially from immediately preoperatively to 48 hours postoperatively to determine if a parallel relationship exists between declining blood gases and altered pulmonary metabolic function. If this relationship exists, we then propose to develop an assay that might allow for the early diagnosis of ARDS and place the diagnosis on a firm biochemical basis.